Search PubMed⌕ Search

Biomedical subjects

I K Smith

Publications and source records attributed to I K Smith.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effect of Plant Growth Regulators on Calcium-stimulated Serine Transport into Tobacco Cells.

The transport of serine into tobacco cells (Nicotiana tabacum L.) cultured in liquid medium was examined. Transport was inhibited approximately 50% by 2,4-dichlorophenoxyacetic acid, indoleacetic acid, alpha-naphthalene acetic acid, and kinetin at a concentration of 10 micrograms per milliliter. Transport was not inhibited by 2,6-dichlorophenoxyacetic acid and inhibited less than 25% by p-chlorophenoxyacetic acid at this concentration. Removal of 2,4-dichlorophenoxyacetic acid from the transport medium resulted in an alleviation of inhibition. Gibberellic acid at concentrations from 2 to 20 micrograms per milliliter stimulated transport.It was previously shown that inhibition of transport by La(3+) was due to removal of Ca(2+) from surface sites and inhibition of Ca(2+) uptake by cells. None of the growth regulators tested had any significant effect on Ca(2+) binding and/or transport.A contributing factor to the low transport rates in the absence of Ca(2+) is the increased rate of serine efflux. None of the growth regulators tested had any significant effect on the rate of serine efflux.

Journal Article↗
PubMed1977

Intrarenal distribution of plasma flow in cirrhosis as measured by transit renography: relationship with plasma renin activity, and sodium and water excretion.

1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]- iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.

Adult↗
PubMed1977

Cysteine transport into cultured tobacco cells.

Cysteine transport by tobacco cells (Nicotiana tabacum L. var. Xanthi) cultured on liquid B-5 medium was examined.Transport was linear with time or amount of tissue and had a pH optimum of 4.5. Cysteine transport over a wide concentration range was biphasic. The isotherm, for descriptive convenience, was divided into two segments both of which obeyed Michaelis-Menten kinetics. The Km for high affinity transport was in the range 1.7 x 10(-5)m(+/-0.17) while the Km for low affinity transport was in the range 3.5 x 10(-4)m(+/-0.13). Maximum velocities were 3 to 6 nmoles/g fresh weight/minute and 13 to 16 nmoles/g fresh weight/minute, respectively.Azide and 2,4-dinitrophenol caused more than 90% inhibition of net transport by either system. N,N'-Dicyclohexylcarbodiimide was not inhibitory while the inhibition by carbonylcyanide m-chlorophenylhydrazone was dependent on the cysteine concentration. Only those compounds that were inhibitory to transport caused significant efflux of labeled material from preloaded cells.Tobacco cells that had been preincubated in iodoacetamide or N-ethylmaleimide did not transport cysteine while similar treatments with dithiothreitol were only slightly inhibitory or had no effect on transport.Transport by either system was, to some extent, inhibited by all other tested amino acids and analogs. Alanine, methionine, and S-methyl cysteine were most effective in inhibiting cysteine transport. Both alanine and methionine were competitive inhibitors of cysteine transport by either system with inhibition constants that were similar to the Km for the particular system.

Journal Article↗
PubMed1977

Effect of beta adrenergic blocking drugs on the renin-aldosterone system, sodium excretion, and renal hemodynamics in cirrhosis with ascites.

As a result of effective beta adrenergic blockade with either propranolol or practolol, plasma renin activity was suppressed in all of 11 patients with cirrhosis and ascites. In contrast, the effect on the rate of renal excretion of aldosterone was variable, suggesting that factors other than the renin-angiotension system are responsible for the control of aldosterone secretion in cirrhosis. The changes in aldosterone could not be explained on the basis of changes in the plasma concentrations of potassium or sodium. The renal sodium excretion was inversely related to the values for aldosterone both before and after beta adrenergic blockade, indicating a major role for aldosterone in regulating sodium excretion. A number of patients had an abnormal intrarenal distribution of plasma flow with a relative hypoperfusion of the renin-secreting outer cortical nephrons. Plasma renin activity was inversely related to outer cortical plasma flow, suggesting that the reduced outer cortical flow may be a stimulus to increased renin secretion. Because the abnormal intrarenal hemodynamic pattern was not corrected by suppression of plasma renin activity, and presumably angiotension II concentrations, it is unlikely that it is attributable to the known renal vasonconstrictor effects of angiotensin II.

Adrenergic beta-Antagonists↗
PubMed1976

The nature of the beta-adrenoreceptor controlling plasma renin activity in man.

1. Seven healthy sodium-replete male volunteer subjects remained supine during and for at least 1 h before the study. Heart rate and blood pressure were recorded continuously, and peripheral venous blood samples were taken every 15 min for determinations of plasma renin activity. 2. All subjects were studied twice: after 3 days of oral practolol (100 mg, three times daily) and after a similar period on placebo. Each study consisted of an intravenous infusion of isoprenaline in graded doses (0-20 microng/min in the placebo phase; 0-16 microng/min in the practolol phase), followed after rest for 2 h by an intravenous infusion of salbutamol (0-20 microng/min after placebo; 0-80 microng/min after practolol). 3. Both salbutamol and isoprenaline produced dose-related increases in systolic blood pressure, heart rate and plasma renin activity and decreases in diastolic pressure. 4. The increases in heart rate and plasma renin activity induced by either agonist were competitively blocked by practolol, as was the fall in diastolic blood pressure induced by isoprenaline; the salbutamol-induced fall of diastolic blood pressure was unaffected by practolol. 5. Comparison of dose ratio--1 estimates confirmed that practolol selectively blocked increases in heart rate and plasma renin activity due to salbutamol; no selective blockade against isoprenaline-induced changes was shown. 6. Selective blockade of salbutamol-induced changes indicate that a beta1-adrenoreceptor mediates changes in plasma renin activity.

Albuterol↗
PubMed1976

Characterization of sulfate transport in cultured tobacco cells.

Sulfate transport by tobacco cells (Nicotiana tabacum L. var. Xanthi) cultured in liquid medium was investigated.Transport was linear with time, had a sharp pH optimum between 6.5 and 7.5, and obeyed Michaelis-Menten kinetics. The Km varied within the range 2 x 10(-5)m and 4 x 10(-5)m and the maximum velocity was in the range 100 to 400 nanomoles per gram fresh weight.hour.Transport was inhibited more than 90% by 10(-4)m sulfite, thiosulfate, metabisulfite, sulfide, selenate, and chromate, but was inhibited less than 40% by 10(-3)m chloride, nitrate, or phosphate. Selenate was a competitive and sulfide a noncompetitive inhibitor of sulfate transport.The oxidative respiration inhibitors, azide and cyanide, uncoupling reagents, carbonylcyanide m-chlorophenylhydrazone (CCCP) and dinitrophenol, and the ATPase inhibitor N,N'-dicyclohexylcarbodiimide (DCCD) were all potent inhibitors of transport. Inhibition by CCCP was not prevented by preincubation of cells with dithiothreitol. Removal of CCCP from the transporting medium resulted in a partial resumption of transport, in contrast removal of DCCD had no effect.Sulfate transport was inhibited more than 90% by 10(-4)m mercaptoethanol, dithiothreitol, or d-cysteine and was abolished by either 10(-5)m N-ethylmaleimide or 10(-4)m iodoacetamide. Removal of mercaptoethanol from the transporting medium resulted in a return to maximal rates of transport whereas when either N-ethylmaleimide or iodoacetamide were removed transport remained inhibited.N-ethylmaleimide (10(-5)m) and iodoacetamide (10(-4)m), which inhibited transport completely, induced the efflux of between 70 and 90% of the transported sulfate in 5 hours. Metabolite efflux was induced by the following compounds, which are listed according to their effectiveness, DCCD, CCCP, mercaptoethanol, and selenate. Increasing the concentration of an inhibitor, in excess of that required to inhibit transport 100%, increased the rate of nonspecific metabolite efflux from the cells.

Journal Article↗
PubMed1975

Sulfate transport in cultured tobacco cells.

Sulfate transport by tobacco (Nicotiana tabacum L. var. Xanthi) cells cultured on either l-cysteine or sulfate as a sole sulfur source was measured. The transport rate on either sulfur source was low during pre-exponential growth, increased during exponential growth, and was maximal in late exponential cells. The initial increase in transport rate was correlated with a decline in the intracellular sulfate, but was not correlated with the amino acid content of the cells which remained relatively constant before the depletion of the endogenous sulfate pool. The previously reported inhibition of sulfate transport by l-cysteine was shown to be caused by an elevation in intracellular sulfate resulting from the degradation of cysteine to sulfate. It is proposed that the intracellular sulfate pool is the major factor regulating the entry of sulfate into tobacco cells.

Journal Article↗
PubMed1972

Studies of l-Cysteine Biosynthetic Enzymes in Phaseolus vulgaris L.

In higher plants the biosynthesis of l-cysteine from l-serine, acetylCoA, and sulfide requires serine transacetylase and O-acetylserine sulfhydrylase. The distribution of these enzymes in kidney bean (Phaseolus vulgaris L. cv. Red Kidney) seedlings was determined. Between one-third and two-thirds of the serine transacetylase activity was associated with mitochondria, whereas all of the O-acetyl-serine sulfhydrylase activity was present in the soluble fraction of cell homogenates. In a 14-day plant approximately two-thirds of the O-acetylserine sulfhydrylase activity and approximately one-half of the serine transacetylase activity was found in the leaves.Sulfur-deficient plants were grown to determine the effect of sulfur status on the levels of cysteine biosynthetic enzymes. Total extractable serine transacetylase activity was not affected by sulfur deficiency; in contrast, there was an increase in O-acetylserine sulfhydrylase activity under these conditions.

Journal Article↗
PubMedDate not supplied

Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis.

The generally held views that plasma renin activity (PRA) is increased in cirrhosis and that this is secondary to reductions in the "effective" blood or extracellular fluid (ECF) volumes, consequent on the effects of portal hypertension, were re-examined in the present study. Measurements of PRA in 67 patients representing different clinical stages of cirrhosis showed that the mean value in 15 patients without ascites was significantly reduced. In 21 of 35 with ascites, PRA was either reduced or within the normal range. A low plasma renin substrate concentration was not the cause for the low PRA. These findings are not in keeping with the concepts of reduced "effective" blood or ECF volumes at least for the majority of patients at these stages of cirrhosis under the conditions of the present study. The only group showing a significantly increased PRA had evidence of renal impairment. In these 17 patients the underlying reduction in renal perfusion may have been the stimulus to the kidney that led to an increase to renin secretion.

Adult↗